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THU0163 Cortisol and prolactin levels in rheumatoid arthritis and systemic lupus erythematosus
  1. E Grabocka,
  2. A Tafaj,
  3. A Këlliçi
  1. Clinic of Reumatology, Hospital University Center “Mother Theresa”, Tirana, Tirana

Abstract

Background Accumulated evidence suggests the existence of bidirectional communication between the neuroendocrine and immune systems. The pituitary gland can regulate the immune response secreting both immunostimulatory [e.g. prolactin (PRL)] and immunosupressive (cortisol via ACTH) hormones. A disorder of the immunoregulatory circuit between these systems could potentially result in the development of immune mediated diseases. Hiperprolactinemia has been implicated in the pathogenesis of systemic lupus erythematosus (SLE), Reiter’s Syndrome and psoriatic arthritis. Elevated PRL levels have been described in patients with rheumatoid arthritis (RA). However, clinical studies regarding the PRL level and disease activity have yielded contradictory results.

Objectives In this study our aim was to assess prolactin and cortisol plasma levels in patients with RA and SLE and to evaluate their correlation with disease activity.

Methods PRL and cortisol plasma levels were measured in 40 female patients aged (24 RA patients and 16 SLE patients) 38.88 ± 14.44 and 40 age-matched healthy controls. Pregnant patients, patients taking drugs that could increase PRL or cortisol levels and those with renal and/or hepatic failure, were excluded from the study. All subjects were premenopausal women with regular menstrual cycles. Plasma concentrations of prolactin and cortisol were determined by radioimmunoassay under standardised conditions in venous blood drawn through an indwelling cannula. Disease activity was assessed using the Disease Activity Score (DAS) for the RA patients SLEDAI for SLE patients.

Results The mean PRL plasma level was higher in RA and SLE than in the control group (13.8 ± 6.1; 15.6 ± 4.2 vs. 8.78 ± 2.43, respectively, p < 0.05). Cortisol plasma levels were found to be higher in the RA and SLE patients than in controls, but there were not significantly different (14.2 ± 3.6; 16.3 ± 3.3 vs. 13.1 ± 2.8 respectively, p > 0.05).

Conclusion No difference was found in prolactin and cortisol levels between RA and SLE patients.

A correlation between prolactin and cortisol levels was found only in SLE patients (p < 0.05).

No correlation was found between PRL or cortisol levels and disease activity in RA and SLE subjects.

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